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Your search keyword '"Lambert, K"' showing total 15 results
Start Over Author "Lambert, K" Journal journal of investigative dermatology
15 results on '"Lambert, K"'

3. 674 The effective killing of the difficult-to-treat melanomas with the combinations of MCL1 inhibitors S63845/MIK665 plus Navitoclax

Author

Mukherjee, N., primary, Skees, J., additional, Todd, K., additional, West, D., additional, Lambert, K., additional, Robinson, W., additional, Amato, C., additional, Couts, K., additional, Van Gullick, R., additional, MacBeth, M., additional, Nassar, K., additional, Tan, A., additional, Zhai, Z., additional, Fujita, M., additional, Bagby, S., additional, Norris, D., additional, and Shellman, Y., additional

Published
2020
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4. 814 RHOJ knockdown modulates the migration and differentiation of normal human melanocytes and the expression of pro-apoptotic markers after UV exposure

Author

Goldstein, N., primary, Steel, A., additional, Koster, M., additional, Wright, M., additional, Trottier, Z., additional, Jones, K., additional, Gao, B., additional, Ward, B., additional, Lambert, K., additional, Robinson, W., additional, Shellman, Y., additional, Fujita, M., additional, Roop, D., additional, Norris, D.A., additional, and Birlea, S.A., additional

Published
2019
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8. 1187 Activation Of RHOJ signaling in human hair follicle bulge melanocytes is a key-factor In NBUVB induction of vitiligo repigmentation

Author

Goldstein, N., primary, Pakieser, J., additional, Wright, M., additional, Caldwell, C., additional, Krug, A., additional, Koster, M., additional, Jones, K., additional, Gao, B., additional, Ward, B., additional, Venkataraman, S., additional, Lambert, K., additional, Shellman, Y., additional, Fujita, M., additional, Roop, D.R., additional, Norris, D., additional, and Birlea, S., additional

Published
2018
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10. 524 SASH1 is a novel gene involved in human pigmentation disorders

Author

Almeida, A., primary, Lambert, K., additional, Goldstein, N., additional, Birlea, S., additional, Mukherjee, N., additional, Janssen, K., additional, Backos, D., additional, Koster, M., additional, Norris, D., additional, Artinger, K., additional, Pacheco, T., additional, and Shellman, Y., additional

Published
2017
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15. Combining a BCL2 inhibitor with the retinoid derivative fenretinide targets melanoma cells including melanoma initiating cells.

Author

Mukherjee N, Reuland SN, Lu Y, Luo Y, Lambert K, Fujita M, Robinson WA, Robinson SE, Norris DA, and Shellman YG

Subjects
Aldehyde Dehydrogenase metabolism, Apoptosis drug effects, Biomarkers, Tumor metabolism, Cell Line, Tumor, Cell Survival drug effects, Drug Synergism, Drug Therapy, Combination, Humans, Neoplastic Stem Cells drug effects, Piperazines pharmacology, Proto-Oncogene Proteins c-bcl-2 metabolism, Retinoids, Antineoplastic Agents pharmacology, Biphenyl Compounds pharmacology, Fenretinide pharmacology, Melanoma pathology, Neoplastic Stem Cells pathology, Nitrophenols pharmacology, Proto-Oncogene Proteins c-bcl-2 antagonists & inhibitors, Skin Neoplasms pathology, Sulfonamides pharmacology
Abstract

Investigations from multiple laboratories support the existence of melanoma initiating cells (MICs) that potentially contribute to melanoma's drug resistance. ABT-737, a small molecule BCL-2/BCL-XL/BCL-W inhibitor, is promising in cancer treatments, but not very effective against melanoma, with the antiapoptotic protein MCL-1 as the main contributor to resistance. The synthetic retinoid fenretinide N-(4-hydroxyphenyl)retinamide (4-HPR) has shown promise for treating breast cancers. Here, we tested whether the combination of ABT-737 with 4-HPR is effective in killing both the bulk of melanoma cells and MICs. The combination synergistically decreased cell viability and caused cell death in multiple melanoma cells lines (carrying either BRAF or NRAS mutations) but not in normal melanocytes. The combination increased the NOXA expression and caspase-dependent MCL-1 degradation. Knocking down NOXA protected cells from combination-induced apoptosis, implicating the role of NOXA in the drug synergy. The combination treatment also disrupted primary spheres (a functional assay for MICs) and decreased the percentage of aldehyde dehydrogenase (high) cells (a marker of MICs) in melanoma cell lines. Moreover, the combination inhibited the self-renewal capacity of MICs, measured by secondary sphere-forming assays. In vivo, the combination inhibited tumor growth. Thus, this combination is a promising treatment strategy for melanoma, regardless of mutation status of BRAF or NRAS.

Published
2015
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